Over 2% of the population suffers from atopic dermatitis, a chronic, recurrent skin disorder. Immunologic abnormalities and the resultant release of inflammatory mediators play a key part in the pathogenesis of this illness, which is still unknown. Treatment with glucocorticoids has long been the gold standard, although their efficacy is restricted because of their side effects. The 5-lipoxygenase pathway produces leukotrienes (LTB4, LTC4, LTD4, and LTE4), which are metabolites of arachidonic acid. They have a crucial role in inflammatory and atopic diseases. In asthma, LT modulating medications have proven to be effective. The potential efficacy of LT antagonists in atopic dermatitis has recently piqued people’s curiosity.
LTs have been shown to have a function in atopic dermatitis in both in vitro and in vivo studies. 5-lipoxygenase inhibitors and LT receptor antagonists are the two categories of LT-modulating medicines. Because the 5-lipoxygenase inhibitor works at an earlier stage in the LT synthesis pathway, it can affect the production of all LTs, including LTB4, whereas receptor antagonists only affect the cysteinyl LTs, such as LTC4, LTD4, and LTE4. This decrease in LTB4 activity might indicate that employing LT synthesis inhibitors rather than LT receptor antagonists for atopic dermatitis has a therapeutic benefit.
Although there is minimal clinical evidence of the use of LT drugs in atopic dermatitis, early results are promising, and these compounds may one day be used as corticosteroid-free therapies for atopic dermatitis.
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